Fig. 16.36 ). Systolic pressure increases until a maximal systolic pressure is reached at the optimal preload (see
Fig. 16.36 ). If diastolic filling continues beyond this point, the pressure developed will no longer increase. At very high filling pressures, peak pressure development in systole is actually reduced.
At a constant preload, higher systolic pressure can be reached during ventricular contractions by an increase in the afterload (e.g., increasing aortic pressure by restricting the runoff of arterial blood to the periphery). Incremental increases in afterload produce progressively higher peak systolic pressures. However, if the afterload continues to increase, it becomes so great that the ventricle can no longer generate enough force to open the aortic valve. At this point, ventricular systole is totally isometric (i.e., there is no ejection of blood), and thus no change occurs in ventricular volume during systole. The maximal pressure developed by the left ventricle under these conditions is the maximal isometric force that the ventricle is capable of generating at a given preload. At preloads below the optimal filling volume, an increase in preload can yield greater maximal isometric force (see
Fig. 16.36
Preload and afterload depend on certain characteristics of the vascular system and the behavior of the heart. With regard to the vasculature, the degree of venomotor tone and peripheral resistance influences preload and afterload. With regard to the heart, a change in rate or stroke volume can also alter preload and afterload. Hence, cardiac and •Fig. 16.37 Preload and Afterload in a Papillary Muscle. A, Restingstage(noload)intheintactheartjustbeforeopeningoftheAVvalves.B, Preload(PL)intheintactheartattheendofventricularfilling.C, Supportedpreloadplusafterload(AL)intheintactheartjustbeforeopeningoftheaorticvalve.D, Liftingpreloadplusafterloadintheintactheartduringventricularejection,withadecreaseinventricularvolume.PL+ AL,totalload.
vascular factors interact with each other to affect preload and afterload (see
Contractility defines cardiac performance at a given preload and afterload. Contractility determines the change in peak isometric force (isovolumic pressure) at a given initial fiber length (end-diastolic volume). Contractility can be augmented by drugs, such as norepinephrine or digitalis, or by an increase in contraction frequency (tachycardia). The increase in contractility (positive inotropic effect) produced by these interventions is reflected by incremental increases in the force developed and in the velocity of contraction.
Indices of Contractility
A reasonable index of myocardial contractility can be derived from the contour of ventricular pressure curves (
Fig. 16.38 ). A hypodynamic heart is characterized by elevated end-diastolic pressure, slowly rising ventricular pressure, and a somewhat reduced ejection phase (curve C in
Fig. 16.38 ). A hyperdynamic heart (curve B in
Fig.
16.38 ) is characterized by reduced end-diastolic pressure, fast-rising ventricular pressure, and a brief ejection phase. The slope of the ascending limb of the ventricular pressure curve indicates the maximal rate of force development by the ventricle. The maximal rate of change in pressure with time—that is, the maximum dP/dt—is illustrated by the tangents to the steepest portion of the ascending limbs of the ventricular pressure curves in
Fig. 16.38 . The slope of the ascending limb is maximal during the isovolumic phase of systole (see
Fig. 16.38 ). At any given degree of ventricular filling, the slope provides an index of the initial contraction velocity and hence an index of contractility.
Similarly, the contractile state of the myocardium can be calculated from the velocity of blood flow that occurs initially in the ascending aorta during the cardiac cycle (
Fig.